Current Projects: National Institutes of Health (NINR, NHLBI)

Neurobehavioral Effects of Partial Sleep Deprivation[NINR]

Principal Investigator: David F. Dinges, Ph.D.

This project continues an innovative line of research on how to optimally use sleep as an intervention to promote cognitive recovery from, and resistance to, the neurobehavioral risks posed by chronic partial sleep deprivation. Chronic insufficient sleep is estimated to affect at least 20% of adults. It can result from medical conditions and sleep disorders, as well as work demands, and social or domestic responsibilities. It is associated with significant clinical morbidity, and directly causes errors and accidents that are due to its adverse neurobehavioral effects on alertness, mood, and cognitive functions.

In seminal experiments conducted under this grant, we showed that the neurobehavioral effects of chronic sleep restriction accumulate to severe levels in a few days, without the full awareness of the affected individuals, and that recovery from chronic sleep restriction requires more sleep than previously assumed. We also discovered that recovery from chronic sleep was illusory, because it masked a heightened neurobehavioral vulnerability to even a single post-recovery night of sleep restriction. The implications of these findings are that apparent recovery from chronic sleep restriction masks a more severe cognitive response to subsequent sleep restriction suggesting that there are longer time constants in the brain for neurobehavioral recovery from chronic sleep restriction. In light of this finding, we now seek to determine whether additional nights of extended recovery sleep will reduce the heightened vulnerability induced by prior exposure to sleep restriction.

A total of 110 adults will be studied in the laboratory during a 17-day protocol evaluating cognitive, psychological and physiological responses to varying recovery days between two sleep-restriction periods. The results will establish the number of nights of recovery sleep needed to prevent accelerated deterioration during a subsequent period of sleep restriction. The findings will advance theoretical understanding of sleep homeostasis and its relationship to cognitive functions, as well as inform theories of sleep need, and have substantial implications for sleep biology, for the treatment of clinical disorders that regularly disrupt sleep, and for managing lifestyle factors that frequently restrict sleep.

Sleep loss increases sleep propensity, destabilizes the wake state, impairs psychomotor and cognitive performance, and causes considerable social, financial and health-related costs. Although insufficient sleep is a risk factor for obesity, cardiovascular disease and diabetes, depression, and prospective mortality, about 20% to 40% of the US adults sleep less than the minimum sleep duration (7-8 hours per night) to prevent cumulative deterioration in cognitive performance. Neurobehavioral evidence from our previous studies and other groups has indicated robust and highly replicable (trait-like) individual differences in the magnitude of sleepiness and cognitive performance vulnerability to sleep deprivation.

While some healthy adults show substantial cognitive deficits during sleep loss, others show few cognitive changes when sleep is deprived. However, little is known about why some sleep-deprived people are more prone to cognitive deficits that can result in costly errors and accidents. To answer this question, we propose to combine our interdisciplinary expertise in neuroimaging and neurobehavioral effects of sleep deprivation to elucidate the neural basis underlying this differential cognitive vulnerability. We will use a new technique of arterial spin labeling (ASL) perfusion functional magnetic resonance imaging (fMRI) for quantification of resting brain activity without task and tonic activation during performance of the psychomotor vigilance test (PVT) in a large sample of N=60 healthy subjects after normal sleep and following sleep deprivation. PVT is a simple, reliable and highly sensitive task for measuring attentional and performance deficits due to sleep deprivation. We will also use traditional BOLD fMRI for measuring phasic activation during fast and slow PVT responses and functional connectivity analysis for studying brain connectivity after normal sleep and following sleep deprivation.

The findings from this project will elucidate the neural mechanisms by which sleep deprivation affects behavioral performance and how the effects of sleep deprivation vary across individuals of differential vulnerability. The new knowledge gained from this study will have relevance for understanding and managing excessive sleepiness due to a number of common sleep disorders (e.g., sleep apnea and other sleep disorders; affective disorders; shift work sleep disorder). The project also has the potential to yield brain-based biomarkers that can be used to predict individual responses to sleep deprivation and its treatment.